Obesity is an independent risk factor for non‐alcoholic fatty liver disease: evidence from a meta‐analysis of 21 cohort studies

Li, L.; Liu, D. W.; Yan, Hong-tao; Wang, Z. Y.; Zhao, Shihua; Wang, B.

doi:10.1111/obr.12407

Cited by 331 publications

(235 citation statements)

References 72 publications

(135 reference statements)

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“…In prospective longitudinal studies, the presence of NAFLD has been associated with an increased risk of cardiovascular disease (CVD) and type 2 diabetes (T2DM); however, it remains unclear whether NAFLD is causally related to these conditions or, rather, it is just an epiphenomenon of other cardiometabolic factors causally related to CVD and T2DM . In fact, the rising prevalence of NAFLD concurs with that of overweight and obesity (particularly visceral fat) . Moreover, as excess body weight is also a risk factor for CVD and T2DM, it has been argued that the associations of NAFLD with CVD and T2DM could be spurious (ie, non‐causal) and reflect the link between overweight/obesity with CVD and T2DM .…”

Section: Introductionmentioning

confidence: 99%

Causality between non‐alcoholic fatty liver disease and risk of cardiovascular disease and type 2 diabetes: A meta‐analysis with bias analysis

Morrison

Zaccardi

Khunti

et al. 2018

Liver International

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Background & Aims A causal association of non‐alcoholic fatty liver disease (NAFLD) with cardiovascular disease (CVD) and type 2 diabetes (T2DM) remains unproved. We aimed to quantify the likelihood of causality examining the sensitivity of observational associations to possible confounding. Methods Studies investigating longitudinal associations of NAFLD with CVD or T2DM were searched on 5 June 2018. Study‐specific relative risks (RRs) were combined in random‐effects meta‐analyses and pooled estimates used in bias analyses. Results Associations of NAFLD with CVD and T2DM were reported in 13 (258 743/18 383 participants/events) and 20 (240 251/12 891) studies respectively. Comparing patients with NAFLD to those without, the pooled RR was 1.48 (95% CI: 0.96, 2.29) for CVD and 2.17 (1.77, 2.65) for T2DM. In bias analyses, for an unmeasured confounder associated to both NAFLD and CVD with a RR of 1.25, the proportion of studies with a true (causal) effect of NAFLD on CVD surpassing a RR of 1.10 (ie, 10% increased risk of CVD in participants with NAFLD) was 0.67 (95% CI: 0.42, 0.92) while for 75% increase, it was 0.36 (0.11, 0.62). Corresponding figures for T2DM were 0.97 (0.91, 1.00) for a 10% increased risk of T2DM in participants with NAFLD to 0.70 (0.49, 0.92) for a 75% increase. Conclusions The results of this study are strongly suggestive for a causal relationship between NAFLD and T2DM, while the evidence for a causal link between NAFLD and CVD is less robust. Therapeutic strategies targeting NAFLD are likely to reduce the risk of developing T2DM.

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Section: Introductionmentioning

confidence: 99%

Causality between non‐alcoholic fatty liver disease and risk of cardiovascular disease and type 2 diabetes: A meta‐analysis with bias analysis

Morrison

Zaccardi

Khunti

et al. 2018

Liver International

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show abstract

“…Cause and gender-specific data on relative risks (along with 95% Confidence Intervals) for 16 diagnoses were obtained from a Canadian cost of illness study based on meta-analyses [17] and from a more recent meta-analyses for type II diabetes [18], non-alcoholic fatty liver disease [19] and gout [20], the latter two diagnosis specific risks being based on average BMI levels of 27.3 and 33.6 in Israeli overweight and obese persons respectively [21]. …”

Section: Methodsmentioning

confidence: 99%

Mortality, hospital days and treatment costs of current and reduced sugar consumption in Israel

Ginsberg

2017

Isr J Health Policy Res

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BackgroundConsumption of sugar causes tooth decay, overweight and obesity related morbidities. This paper in response to the Minister of Health’s request, provides estimates of the mortality, morbidity and health care costs attributable to sugar consumption in Israel along with the effects of reducing sugar consumption.MethodsGender specific relative risks of many diseases from overweight (25 < =BMI < 30) and obesity (BMI > =30) were applied to the national gender specific prevalence rates of overweight and obesity in order to calculate the population attributable fraction (PAF) from overweight and obesity. National expenditure on these related diseases was calculated by applying disease-specific data from a recent Canadian study to estimates of disease specific general hospital expenditures in Israel. Disease specific costs attributable to overweight and obesity were estimated from the product of these expenditures and PAF. In addition national costs of treating caries in persons under 18 years of age from sugar were calculated. Similar calculations were made to estimate the burden from sugar in terms of mortality and hospital utilisation. A recent UK modelling study was used to estimate the effect of a national program to reduce calorific consumption of sugar from 12.45 to 10% in 5 years.ResultsConditions associated with overweight or obesity accounted annually for 6402 deaths (95% CI 3296–8760) and 268,009 hospital days. Dental costs attributable to sugar consumption were 264 million NIS. In total, obesity, overweight and sugar consumption accounted for 2449 million in direct treatment costs (0.21% of GDP), rising to 4027 million (0.35% of GDP) when indirect costs were included. A national program of reducing energy from sugar consumption from 12.45 to 10% over 5 years is considered have a very feasible short-term goal. Even if the program does not impose taxes on sugar consumption, this would save 778 million NIS as well as 1184 lives.ConclusionSugar consumption causes a huge monetary and mortality burden. Estimates of potential decreases in this burden justify the current prioritisation given by the health minister of creating and implementing a national program to reduce sugar consumption, which is likely to be cost-saving (ie: averted treatment costs will exceed intervention costs).

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“…Obesity is closely associated with diabetes, nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH), and cardiovascular diseases (64). Numerous studies have reported that dysregulation of sphingolipid metabolism is linked to diabetes (4).…”

Section: Sphks and S1p In Lipid Metabolismmentioning

confidence: 99%

Sphingosine Kinases/Sphingosine 1-Phosphate Signaling in Hepatic Lipid Metabolism

Kwong

Hylemon

et al. 2017

Curr Pharmacol Rep

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The ever-increasing prevalence of metabolic diseases such as dyslipidemia and diabetes in the western world continues to be of great public health concern. Biologically active sphingolipids, such as sphingosine 1-phosphate (S1P) and ceramide, are important regulators of lipid metabolism. S1P not only directly functions as an active intracellular mediator, but also activates multiple signaling pathways via five transmembrane G-protein coupled receptors (GPCRs), S1PR1-5. S1P is exclusively formed by sphingosine kinases (SphKs). Two isoforms of SphKs, SphK1 and SphK2, have been identified. Recent identification of the conjugated bile acid-induced activation of S1PR2 as a key regulator of SphK2 opened new directions for both the sphingolipid and bile acid research fields. The role of SphKs/S1P-mediated signaling pathways in health and various human diseases has been extensively reviewed elsewhere. This review focuses on recent findings related to SphKs/S1P-medaited signaling pathways in regulating hepatic lipid metabolism.

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Obesity is an independent risk factor for non‐alcoholic fatty liver disease: evidence from a meta‐analysis of 21 cohort studies

Abstract: Obese individuals have a 3.5-fold increased risk of developing NAFLD, and there is an obvious dose-dependent relationship between BMI and NAFLD risk. © 2016 World Obesity.

Cited by 331 publications

References 72 publications

Causality between non‐alcoholic fatty liver disease and risk of cardiovascular disease and type 2 diabetes: A meta‐analysis with bias analysis

Causality between non‐alcoholic fatty liver disease and risk of cardiovascular disease and type 2 diabetes: A meta‐analysis with bias analysis

Mortality, hospital days and treatment costs of current and reduced sugar consumption in Israel

Sphingosine Kinases/Sphingosine 1-Phosphate Signaling in Hepatic Lipid Metabolism

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